ATTENUATED GLYCINE RECEPTOR FUNCTION REDUCES EXCITABILITY OF MOUSE MEDIAL VESTIBULAR NUCLEUS NEURONS
ATTENUATED GLYCINE RECEPTOR FUNCTION REDUCES EXCITABILITY OF MOUSE MEDIAL VESTIBULAR NUCLEUS NEURONS
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DOI：
10.1016/j.neuroscience.2010.06.040
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发表时间：
2010-09-29
期刊：
影响因子：
3.3
通讯作者：
Brichta, A. M.
中科院分区：
文献类型：
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作者：
Camp, A. J.;Lim, R.;Brichta, A. M.
内侧前庭核（MVN）神经元的自发活动受突触输入的调节。这些输入对于维持凝视和姿势至关重要，并有助于外周前庭器官损伤后的前庭代偿。我们研究了慢性减弱的甘氨酸能输入如何影响MVN神经元的兴奋性。为此，我们使用了三种小鼠品系（痉挛型、阵挛型和振荡型），它们在抑制性甘氨酸受体（GlyR）上具有特征明确的自然发生突变。首先，通过全细胞膜片钳记录，我们证明突变小鼠的MVN神经元对快速施加甘氨酸的反应幅度显著降低了25% - 90%。接下来我们确定GlyR功能降低如何影响MVN神经元的输出。神经元通过两种模式进行分类：（1）其动作电位后超极化（AHP）的形状；（2）对超极化电流注入的反应。在第一种模式中，神经元被分为A、B和C型。突变品系中C型神经元的比例显著增加。在第二种模式中，缺乏抑制后反弹发放（PRF缺失）的神经元比例增加。在这两种模式中，AHP幅度增加是突变品系中增加的神经元组（C型，PRF缺失）的一个共同特征。我们认为AHP幅度增加会降低MVN的整体兴奋性，从而在甘氨酸能输入减少的环境中维持网络功能。（C）2010国际脑研究组织。由爱思唯尔有限公司出版。保留所有权利。
Spontaneous activity in medial vestibular nucleus (MVN) neurons is modulated by synaptic inputs. These inputs are crucial for maintaining gaze and posture and contribute to vestibular compensation after lesions of peripheral vestibular organs. We investigated how chronically attenuated glycinergic input affects excitability of MVN neurons. To this end we used three mouse strains (spastic, spasmodic, and oscillator), with well-characterized naturally occurring mutations in the inhibitory glycine receptor (GlyR). First, using whole-cell patch-clamp recordings, we demonstrated that the amplitude of the response to rapidly applied glycine was dramatically reduced by 25 to 90% in MVN neurons from mutant mice. We next determined how reduced GlyR function affected MVN neuron output. Neurons were classified using two schemas: (1) the shape of their action potential afterhyperpolarization (AHP); and (2) responses to hyperpolarizing current injection. In the first schema, neurons were classified as types A, B and C. The prevalence of type C neurons in the mutant strains was significantly increased. In the second schema, the proportion of neurons lacking post inhibitory rebound firing (PRF-deficient) was increased. In both schemas an increase in AHP amplitude was a common feature of the augmented neuron group (type C, PRF-deficient) in the mutant strains. We suggest increased AHP amplitude reduces overall excitability in the MVN and thus maintains network function in an environment of reduced glycinergic input. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.